Pancreatic Cancer Tumor Homograft Models

Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year survival rate and remains one of the most difficult to treat cancer types, with very few standard of care options. Unfortunately, ICI have achieved limited clinical benefits as single agent treatments and combinatory therapy evaluation warrant relevant preclinical models. KPC models, first described by Tuveson and colleagues(1) as LSL-KrasG12D/+; LSL-Trp53R172H/+; Pdx1-Cre, and later established as a variety of derivatives by several labs, recapitulate human PDAC tumors in morphology and immune phenotype, and their resistance to a series of chemotherapies and immune checkpoint inhibitors. Our suite of pancreatic tumor homografts all preserve KRAS activating mutations and TP53 loss, and our KPC homografts retain morphological similarity to the original GEMM, making them the ideal models for interrogating combination strategies.

MODEL CANCER TYPE ORIGINAL GEMM MUTATION models per page
mPA6059Pancreatic CancerKRAS (G12D); P53-/-VIEW MODEL
mPA6063Pancreatic CancerKRAS (G12D); P53-/-VIEW MODEL
mPA6114Pancreatic CancerKRAS (G12D); P53-/-;Pdx-1 creVIEW MODEL
mPA6115Pancreatic CancerKRAS (G12D); P53-/-;PDx-1 creVIEW MODEL
mPA6175Pancreatic CancerKRAS (G12D); P53-/-VIEW MODEL
mPA6179Pancreatic CancerKRAS (G12D); P53-/-VIEW MODEL